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On the mechanism underlying the divergent retinal and bristle defects of M8* ( E(spl)D ) in Drosophila
Author(s) -
Kahali Bhaskar,
Bose Anasua,
Karandikar Umesh,
Bishop Clifton P.,
Bidwai Ashok P.
Publication year - 2009
Publication title -
genesis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.093
H-Index - 110
eISSN - 1526-968X
pISSN - 1526-954X
DOI - 10.1002/dvg.20521
Subject(s) - bristle , psychological repression , phosphorylation , biology , microbiology and biotechnology , mutant , endogeny , ectopic expression , transgene , drosophila (subgenus) , genetics , biochemistry , gene , gene expression , brush , electrical engineering , engineering
Our results, using endogenous mutants and Gal4‐ UAS driven transgenes, implicate multisite phosphorylation in repression by E(spl)M8. We propose that these phosphorylations occur in the morphogenetic furrow (MF) to reverse an auto‐inhibited state of M8, enabling repression of Atonal during R8 specification. Our studies address the paradoxical behavior of M8*, the truncated protein encoded by E(spl)D . We suggest that differences in N signaling in the bristle versus the eye underlie the antimorphic activity of M8* in N + (ectopic bristles) and hypermorphic activity in N spl (reduced eye). Ectopic M8* impairs eye development (in N spl ) only during establishment of the atonal feedback loop (anterior to the MF), but is ineffective after this time point. In contrast, a CK2 phosphomimetic M8 lacking Groucho (Gro) binding, M8SDΔGro, acts antimorphic in N + and suppresses the eye/R8 and bristle defects of N spl , as does reduced dosage of E(spl ) or CK2. Multisite phosphorylation could serve as a checkpoint to enable a precise onset of repression, and this is bypassed in M8*. Additional implications are discussed. genesis 47:456–468, 2009. © 2009 Wiley‐Liss, Inc.